Peripheral nerve stimulation to treat auditory dysfunction

ABSTRACT

A system and/or method for treating auditory dysfunction by somatosensory system stimulation. The system and/or method comprises a probe and a device to stimulate the probe. The probe has a stimulation portion implanted in communication with a predetermined peripheral nerve site. The stimulation portion of the probe may be implanted in contact with a peripheral nerve dorsal root ganglia, cranial nerve or dermatome area, for example C2 dermatome area or a trigeminal dermatome area. The stimulation portion may be a laminotomy, paddle, surgical, or multiple electrode lead. The device to stimulate the probe may be implanted subcutaneously or transcutaneously.

RELATED APPLICATIONS

This application claims priority to U.S. Provisional Application Nos.60/620,827 filed Oct. 21, 2004 and 60/631,091 filed Nov. 24, 2004 eachof which is incorporated herein by reference in its entirety.

This application is also related to U.S. Provisional Application Nos.60/620,762 filed Oct. 21, 2004, 60/631,085 filed Nov. 24, 2004,60/620,847 filed Oct. 21, 2004, 60/631,089 filed Nov. 24, 2004,60/639,365 filed Dec. 27, 2004 each of which is incorporated byreference in its entirety.

TECHNICAL FIELD

This invention relates to neuronal tissue stimulation for medicaltreatment, and more particularly to stimulating peripheral nerves totreat auditory dysfunction.

BACKGROUND OF THE INVENTION

Hearing clarity is taken for granted by most people; however, temporaryperiods of altered auditory perception are a normal part of existence.Nearly every individual will experience phantom noises such as “ringingin the ears” during their lifetime as a result of exposure to externaland/or internal stimuli. Loud noise (reported by Zhang et al.,Wallhausser-Franke et al.), certain pharmaceuticals, stress, and variousphysical conditions can all cause altered auditory perception, usuallyon a temporary basis. However, for some individuals with auditorydysfunction, altered auditory perception can be permanent.

Auditory dysfunctions are common. For example, in the United States, theprevalence of tinnitus when the whole population is considered isapproximately 3%. This prevalence is only 1% under the age of 45 butincreases significantly with age, rising to 9% in the population over 65years (Adams et al., 1999). This roughly translates to 36 millionAmericans with tinnitus (Heller 2003). Tinnitus is a noise in the ears,often described as ringing, buzzing, roaring, or clicking. Subjectiveand objective forms of tinnitus exist, with objective tinnitus oftencaused by muscle contractions or other internal noise sources in thearea proximal to auditory structures. In certain cases, externalobservers can hear the sound generated by the internal source ofobjective tinnitus. In subjective forms, tinnitus is audible only to thesubject. Tinnitus varies in perceived amplitude, with some subjectsreporting barely audible forms and others essentially deaf to externalsounds and/or incapacitated by the intensity of the perceived noise.

Because auditory dysfunction often occurs secondary to a pathologicalstate, initial treatment may focus on finding an underlying cause. Asubject presenting with, for example, tinnitus may be asked forinformation regarding medications, recent or chronic noise exposure, andhome and work environment. Common medications such as aspirin are knownto cause tinnitus in some patients or in elevated dosages. Stress can bea direct cause of tinnitus and can aggravate existing cases. A thoroughphysical exam is typically made of a subject with complaints of tinnitusto eliminate pathologies such as hypertension, tumors, and infections.Objective tinnitus may be diagnosed using a stethoscope if the source ofthe noise can be localized. For example, hypertension or arterialdisorders may produce objective tinnitus, as the carotid arteries passclose to the auditory organs in humans, and excessive pressure orarterial blockage may cause detectible noise to both the subject and toan outside observer.

If a treatable underlying cause to auditory dysfunction symptoms isidentified, treatment may focus on elimination of the cause. Forexample, hypertensive patients may see a reduction or elimination oftinnitus once anti-hypertensive therapy begins. However, a significantnumber of patients have untreatable underlying pathologies or haveauditory dysfunction in the absence of any identifiable cause. For thesepatients, treatments for directly reducing or eliminating the auditorydysfunction are desirable.

Tinnitus research is actively pursued in the hope of finding efficacioustreatments. Recently published work has utilized drug delivery systemssuch as the system described in U.S. Pat. No. 5,713,847, which includesa catheter inserted into a patient's auditory cortex or thalamus formicroinfusing drugs.

Another example of published drug delivery techniques is U.S. Pat. No.6,656,172, which describes a tinnitus treatment that includes insertingintrathecally a catheter for infusing a drug. Other treatment methodsmay try to mask the perceived tinnitus noise by generating an audiblesignal of appropriate frequency. WO 01/08617 describes a system with avibrating probe placed in proximity to the inner ear.

Nerve stimulation has been shown to be helpful in treating patients withchronic intractable pain. For those patients who prove unresponsive toconservative pain management techniques, peripheral nerve stimulationmay be a successful therapy for pain management when the pain is knownto result from a specific nerve. Peripheral nerve stimulation is basedin part on the Melzack-Wall gate control theory of pain. Sweet andWespic first used electrical stimulation of peripheral nerves in the1960s to mask the sensation of pain with a tingling sensation(paresthesia) caused by the electrical stimulation. Subsequentrefinements in the technology, surgical technique and patient selectionhave led to improved long term results.

The use of certain stimulating electrodes to mask tinnitus has beenpublished. U.S. Pat. Nos. 5,735,885 and 5,496,369 describe the placementof an electrode in the primary auditory cortex of a patient. U.S. Pat.Nos. 6,456,886 and 5,697,975 also use an electrode placed in theauditory cortex, and further describe placement of an electrode in themedial geniculate body of the thalamus.

BRIEF SUMMARY OF THE INVENTION

Peripheral nerves carry both motor and sensory information to and fromthe brain. The present invention comprises a therapeutic system fortreating auditory dysfunction having a surgically implanted device incommunication with a predetermined peripheral nerve. The device caninclude a distal probe, such as, for example, an electrode assembly orelectrical stimulation lead. The proximal end of the probe is coupled toan electrical signal source, which, in turn, is operated to stimulatethe predetermined peripheral nerve.

The predetermined site can be, for example, but not limited to adermatome area, for example, C2, C3, C4, C5, C6, C7, C8, as well as anythoracic, lumbar or sacral dermatome. Cervical nerve roots (e.g., C1,C2, C3, C4, C5, C6, C7 and C8) and cranial nerves (e.g., olfactorynerve, optic, nerve, oculomoter nerve, trochlear nerve, trigeminalnerve, abducent nerve, facial nerve, vestibulocochlear nerve,glossopharyngeal nerve, vagal nerve, accessory nerve, and hypoglossalnerve) to provide therapeutic treatments according to the instantinvention. Other dermatomes that can be included in the presentinvention include dermatomes associated with cranial nerves havingsomatosensory function, for example, but not limited to dermatomesassociated with the trigeminal nerve, intermediate part of the facialnerve, glossopharyngeal nerve, or vagal nerve. Other peripheral nervesare spinal nerves such as the suboccipital nerve, the greater occipitalnerve, the lesser occipital nerve, the greater auricular nerve, thelesser auricular nerve, the phrenic nerve, and the brachial plexus,which branches to form the dorsal scapular nerve, the thoracic nerve,the suprascapular nerve, the lateral pectoral, the musculocutaneousnerve, the axillarily nerve, the radial nerve, the median nerve, theulnar nerve, and other minor peripheral nerves, as well as sympatheticand parasympathetic nerves. Yet further, other peripheral nerves alsoincludes thoracic nerve roots (e.g., T1, T2, T3, T4, T5, T6, T7, T8, T9,T10, T11, T12), lumbar nerve roots (L1, L2, L3, L4, L5) sacral nerveroots (e.g., S1, S2, S3, S4, S5) and the coccygeal nerve.

Embodiments of the invention can operate with various stimulationparameters. One example of stimulation parameters used to treat auditorydysfunctions, such as, for example, tinnitus, may use an amplitude inthe range of about 2 mA to about 100 mA, a frequency in the range ofabout 3 Hz to about 80 Hz, and a pulse width in the range of about 5microseconds to about 100 microseconds. However, other parameters areused in other embodiments of the invention, such as, for example, higherand lower frequencies, various current amplitudes, and/or pulse widthdurations. In another embodiment of the invention, a frequencystimulation parameter of about 80 Hz is used. Burst mode stimulation isused in preferred embodiments of the invention. The burst stimuluscomprises a frequency in the range of about 1 Hz to about 300 Hz, moreparticular, in the range of about 1 Hz to about 12 Hz, and moreparticularly, in the range of about 1 Hz to about 4 Hz, 4 Hz to about 7Hz or about 8 Hz to about 12 Hz, 18 Hz to 20 Hz, and 40 Hz. The burststimulus comprises at least two spikes, for example, each burst stimuluscan comprise about 2 to about 100 spikes, more particularly, about 2 toabout 10 spikes. Each spike can comprise a frequency in the range ofabout 50 Hz to about 1000 Hz, more particularly, in the range of aboutthe range of about 200 Hz to about 500 Hz. The interval between spikescan be about 0.5 milliseconds to about 100 milliseconds. Moreparticularly, the maximum inter-spike interval may be about 5milliseconds. Those of skill in the art realize that this can varydepending upon the patient and the treatment. The frequency of thespikes within the burst does not need to be constant or regular, infact, typically, the frequency of the spikes is random or variable. Infurther embodiments, the burst stimulus is followed by an inter-burstinterval. The inter-burst interval has a duration in the range of about5 milliseconds to about 5 seconds, more preferably, in the range ofabout 10 milliseconds to about 300 milliseconds, or any rangetherebetween. Preferably, the minimum inter-burst interval may be about20 milliseconds. It is envisioned that the burst stimulus has a durationin the range of about 10 milliseconds to about 5 seconds, moreparticularly in the range of about 250 milliseconds to 1 second. Theburst stimulus and the inter-burst interval can have a regular patternor an irregular pattern (e.g., random or irregular harmonics).

Embodiments of the invention also comprise methods for treating auditorydysfunction. The method comprises surgically implanting an electricalstimulation lead such as a laminotomy lead, paddle, surgical, ormultiple electrode lead. Following implantation, the proximal end of thelead is attached to a signal generator. The signal generator thengenerates a signal that stimulates a predetermined peripheral nerve. Thestimulation of the peripheral nerve modulates components of thesomatosensory system that in turn modulate components of the auditorysystem's extralemniscal pathway.

In some embodiments of the invention, the stimulation parameters arevaried after implantation to optimize treatment of an auditorydysfunction. The parameters varied may include modification of thepredetermined implantation site, or modification of, for example, signalamplitude, frequency, pulsewidth or pulse shape of the stimulationsignal.

Other stimulation devices used in certain embodiments are drug pumpswhich provide chemical stimulation of a predetermined peripheral nerve.Chemical stimulation can be provided by delivery of pharmaceuticals orneuroactive substances that, for example, disrupt, block, stimulate,and/or modulate peripheral nerve activity.

Magnetic stimulation of predetermined peripheral nerve sites for thetreatment of auditory dysfunction is used in certain embodiments of thepresent invention. Magnetic stimulation can be provided by internallyimplanted probes or by externally applied directed magnetic fields.

Yet further, thermal stimulation can be provided via implanted probesthat are regulated to heat and/or cold temperatures. In otherembodiments, ultrasound stimulation is used as a stimulation source,either by itself or in combination with another stimulation source. Forexample, in certain embodiments of the invention, ultrasound is used tostimulate active tissue by propagating ultrasound in the presence of amagnetic field as described by Norton (2003), herein incorporated byreference in its entirety. Combinations of stimulation sources are usedin some embodiments of the invention.

The foregoing has outlined rather broadly the features and technicaladvantages of the present invention in order that the detaileddescription of the invention that follows may be better understood.Additional features and advantages of the invention will be describedhereinafter which form the subject of the claims of the invention. Itshould be appreciated that the conception and specific embodimentdisclosed may be readily utilized as a basis for modifying or designingother structures for carrying out the same purposes of the presentinvention. It should also be realized that such equivalent constructionsdo not depart from the invention as set forth in the appended claims.The novel features which are believed to be characteristic of theinvention, both as to its organization and method of operation, togetherwith further objects and advantages will be better understood from thefollowing description when considered in connection with theaccompanying figures. It is to be expressly understood, however, thateach of the figures is provided for the purpose of illustration anddescription only and is not intended as a definition of the limits ofthe present invention.

BRIEF DESCRIPTION OF THE DRAWING

For a more complete understanding of the present invention, reference isnow made to the following descriptions taken in conjunction with theaccompanying drawing, in which:

FIGS. 1A-1B are illustrations of the human auditory system includingneural connections;

FIG. 2 is an illustration of connections in the lemniscal auditorypathway;

FIGS. 3A-3B illustrate example stimulation systems for electricallystimulating peripheral nerves;

FIGS. 4A-4I illustrate example electrical stimulation leads that may beused to electrically stimulate peripheral nerves;

FIG. 5 illustrates implantation of a single stimulation lead near thespinal cord to stimulate a peripheral nerve;

FIG. 6 illustrates an example method of implanting the stimulationsystem of FIGS. 1A-1B with bilateral leads in communication withperipheral nerves; and

FIGS. 7A-7B illustrate examples of the C2 dermatome area; FIG. 7A andFIG. 7B show the cervical dermatomes, including C2 and C3 dermatome.

FIG. 8 shows the anatomy of the occiput or occipital area of a subject'shead. Anatomical structures shown include nerves, muscle and the galea.

FIG. 9 is a block diagram of processes according to a method fortreating auditory dysfunctions such as tinnitus using a peripheral nervestimulation system.

DETAILED DESCRIPTION OF THE INVENTION I. Definitions

Unless defined otherwise, technical and scientific terms used hereinhave the same meaning as commonly understood by one of ordinary skill inthe art to which this invention belongs. For purposes of the presentinvention, the following terms are defined below.

As used herein, the use of the word “a” or “an” when used in conjunctionwith the term “comprising” in the claims and/or the specification maymean “one,” but it is also consistent with the meaning of “one or more”,“at least one”, and “one or more than one.” Still further, the terms“having”, “including”, “containing” and “comprising” are interchangeableand one of skill in the art is cognizant that these terms are open endedterms.

As used herein, the term “auditory dysfunction” refers to conditions ordysfunctions associated with the auditory pathway. Such auditorydysfunctions can include, but are not limited to tinnitus, hyperacousis,phonophobia, misophonia, auditory agnosia in all its forms (verbaland/or non-verbal), auditory spatial dysfunction (localizing sound) andauditory hallucinations, inclusive of musical hallucinosis. Auditoryhallucinations can occur in schizophrenia or use of certain drugs (e.g.,antimuscarinic agents, antiparkinsonian drugs, antidepressants, betaadrenoceptor antagonists and opiates). Auditory dysfunction can alsoinclude hearing loss. Hearing loss can be conductive hearing loss(mechanical transmission of sound into the sensory receptors in thecochlea is impaired), sensorineural hearing loss (a loss of function inthe sensory receptors in either the cochlea or the auditory nerve), orcentral hearing loss (a lesion in the brain stem or auditory cortex).

As used herein, the terms “auditory nerve” and “cochlear nerve” areinterchangeable and refer to the nerve fibers along which the sensorycells of the ear communicate information to the brain. The auditory orcochlear nerve are part of the vestibulocochlear nerve which carries twokinds of sensation, vestibular (balance) and audition (hearing) fromsensory receptors in the inner ear. The auditory nerve consists of thevestibular nerve and the cochlear nerve. The vestibulocochlear nerve isalso known as the eighth cranial nerve.

As used herein, the term “in communication” refers to the stimulationlead being adjacent, in the general vicinity, in close proximity, ordirectly next to or directly on the predetermined stimulation site.Thus, one of skill in the art understands that the lead is “incommunication” with the predetermined site if a stimulation signalresults in a modulation of neuronal activity. For example, thepredetermined site is selected in the present invention such that astimulation lead in communication with a peripheral nerve will stimulatethe peripheral nerve when a stimulation signal is applied to thestimulation lead.

As used herein, the term “dermatome” refers to the area of skininnervated by a single dorsal root. One of skill in the art realizesthat the boundaries of dermatomes are not distinct and in fact overlapbecause of overlapping innervations by adjacent dorsal roots. Dermatomesare divided into sacral (S), lumbar (L), thoracic (T) and cervical (C).Yet further, as used herein, the term “dermatome” includes all theneuronal tissues located within the region or adjacent the dermatomearea, for example, it may include any peripheral nerve, for example, anycervical nerve root (C1, C2, C3, C4, C5, C6, C7 and C8) that mayinnervate the dermatome, any and cranial nerve (e.g., olfactory nerve,optic, nerve, oculomoter nerve, trochlear nerve, trigeminal nerve,abducent nerve, facial nerve, vestibulocochlear nerve, glossopharyngealnerve, vagal nerve, accessory nerve, and hypoglossal nerve) that mayinnervate the dermatome. Other dermatomes that can be included in thepresent invention include dermatomes associated with cranial nerveshaving somatosensory function, for example, but not limited todermatomes associated with the trigeminal nerve, intermediate part ofthe facial nerve, glossopharyngeal nerve, or vagal nerve. Thus, while tosome, dermatomes may have a meaning that relates specifically to sensoryneurons, as used herein, this limitation should not be applied, butrather the broader description used herein should be used.

As used herein, the use of the words “epidural space” or “spinalepidural space” is known to one with skill in the art, and refers to anarea in the interval between the dural sheath and the wall of the spinalcanal.

As used herein, the term “C2 dermatome area” refers to the area or thedermatome that covers the occiput or occipital area and the top portionof the neck. Yet further, C2 dermatome area includes the neuronal tissuethat is located within this area, for example, the C2 dermatome area andits branches innervate the C2 dermatome, as well as any cervical nerveroot and/or cranial nerve that may innervate this area. Thus, the C2dermatome area may also be referred to as the occiput or occipital area,which refers to the back of the head.

As used herein the term “modulate” refers to the ability to regulatepositively or negatively neuronal activity. Thus, the term modulate canbe used to refer to an increase, decrease, masking, altering, overridingor restoring of neuronal activity.

As used herein, the term “burst firing” or “burst mode” or “burst modestimulation” refers to an action potential that is a burst of highfrequency spikes (300-1000 Hz) (Beurrier et al., 1999). Burst firingacts in a non-linear fashion with a summation effect of each spike. Oneskilled in the art is also aware that burst firing can also be referredto as phasic firing, rhythmic firing (Lee 2001), pulse train firing,oscillatory firing and spike train firing, all of these terms usedherein are interchangeable. While not being bound by theory, one ofskill in the art is also aware that the burst stimulus can also bedefined as amplitude modulation (AM) and/or transient frequencymodulation (FM) as it relates to the communication fields.

As used herein, the term “burst” refers to a period in a spike trainthat has a much higher discharge rate than surrounding periods in thespike train (N. Urbain et al., 2002). Thus, burst can refer to aplurality of groups of spike pulses. A burst is a train of actionpotentials that occurs during a ‘plateau’ or ‘active phase’, followed bya period of relative quiescence called the ‘silent phase’ (Nunemaker,Cellscience Reviews Vol 2 No. 1, 2005.) Thus, a burst comprises spikeshaving an inter-spike interval in which the spikes are separated by 0.5milliseconds to about 100 milliseconds. Those of skill in the artrealize that the inter-spike interval can be longer or shorter. Yetfurther, those of skill in the art also realize that the spike ratewithin the burst does not necessarily occur at a fixed rate; this ratecan be variable.

As used herein, the term “tonic firing” or “tonic mode” refers to anaction potential that occurs in a linear fashion.

As used herein, the term “spike” refers to an action potential. Yetfurther, a “burst spike” refers to a spike that is preceded or followedby another spike within a short time interval (Matveev, 2000), inotherwords, there is an inter-spike interval, in which this interval isgenerally about 10 ms but can be shorter or longer, for example 5milliseconds or 0.5 milliseconds.

As used herein, the term “neuronal” refers to a neuron which is amorphologic and functional unit of the brain, spinal cord, andperipheral nerves.

As used herein, the term “peripheral nerve” refers a neuron or a bundleof neurons comprising a part of the peripheral nervous system. Thenervous system comprises two general components, the central nervoussystem, which is composed of the brain and the spinal cord, and theperipheral nervous system, which is composed of ganglia or dorsal rootganglia and the peripheral nerves that lie outside the brain and thespinal cord. One of skill in the art realizes that the nervous systemmay be separated anatomically, but functionally they are interconnectedand interactive. The peripheral nervous system is divided into theautonomic system (parasympathetic and sympathetic), the somatic systemand the enteric system. The term peripheral nerve is intended to includeboth motor and sensory neurons and neuronal bundles of the autonomicsystem, the somatic system, and the enteric system that reside outsideof the spinal cord and the brain. Peripheral nerve ganglia and nerveslocated outside of the brain and spinal cord are also described by theterm peripheral nerve.

As used herein, the term “somatosensory system” refers to the peripheralnervous system division comprising primarily afferent somatic sensoryneurons and afferent visceral sensory neurons that receive sensoryinformation from skin and deep tissue, including the 12 cranial and 21spinal nerves.

As used herein, “spinal cord,” “spinal nervous tissue associated with avertebral segment,” “nervous tissue associated with a vertebral segment”or “spinal cord associated with a vertebral segment or level” includesany spinal nervous tissue associated with a vertebral level or segment.Those of skill in the art are aware that the spinal cord and tissueassociated therewith are associated with cervical, thoracic and lumbarvertebrae. As used herein, C1 refers to cervical vertebral segment 1, C2refers to cervical vertebral segment 2, and so on. T1 refers to thoracicvertebral segment 1, T2 refers to thoracic vertebral segment 2, and soon. L1 refers to lumbar vertebral segment 1, L2 refers to lumbarvertebral segment 2, and so on, unless otherwise specifically noted. Incertain cases, spinal cord nerve roots leave the bony spine at avertebral level different from the vertebral segment with which the rootis associated. For example, the T11 nerve root leaves the spinal cordmyelum at an area located behind vertebral body T8-T9 but leaves thebony spine between T11 and T12.

As used herein, the term “stimulate” or “stimulation” refers toelectrical, chemical, and/or magnetic stimulation that modulates thepredetermined sites in the brain.

As used herein, the term “treating” and “treatment” refers to modulatingcertain areas of the brain so that the subject has an improvement in thedisease, for example, beneficial or desired clinical results. Forpurposes of this invention, beneficial or desired clinical resultsinclude, but are not limited to, alleviation of symptoms, diminishmentof extent of disease, stabilized (i.e., not worsening) state of disease,delay or slowing of disease progression, amelioration or palliation ofthe disease state, and remission (whether partial or total), whetherdetectable or undetectable. One of skill in the art realizes that atreatment may improve the disease condition, but may not be a completecure for the disease.

II. Auditory Pathways

The auditory system comprises components that convert sound pressurewaves into neural impulses that are ultimately processed by the nervoussystem. A simplified version of these components as they appear inhumans is shown in FIG. 1B. Auditory canal 101 channels pressure wavesto tympanic membrane 102 which moves in response to incoming waves.Movement of the tympanic membrane 102 is transmitted to three ossicles103 located in the middle ear. The ossicles 103 amplify the movement ofthe tympanic membrane 102 so that sound vibrations are converted to highpressure sound waves in fluid located in the cochlea 104. In vivo, thecochlea 104 is coiled like a snail shell.

FIG. 1B shows the cochlea 104 of FIG. 1A as it would appear uncoiled.Cochlea 104 is divided into two fluid-filled chambers separated by theorgan of Corti 106. Vibrations in the fluid cause mechanical stimulationof sensory receptor cells known as hair cells on the organ of Corti 106.This mechanical stimulation causes ion channels on the hair cells toopen, altering their membrane potential and changing the release rate ofa synaptic neurotransmitter. Afferent nerve fibers from the auditorynerve 107 take up the neurotransmitter and an action potential in thenerve fibers may be generated depending on the quantity of releasedneurotransmitter. This is a simplified diagram, and other afferent andefferent nerve fibers are also involved in auditory informationcollection and processing.

The auditory nerve connects to two separate pathways after leaving thecochlea. The lemniscal pathway, also known as the classical or specificauditory pathway, is the route taken for signals that humans consciouslyperceive as sound information. The lemniscal is phylogenetically theyoungest of the two pathways. The lemniscal pathway is organizedtonotopically, with specific parts of the pathway carrying informationspecific to received auditory frequencies. It is also linear, such thatthe impulse rate of lemniscal neurons is related to the amplitude ofsound waves detected at the cochlea. The lemniscal pathway isillustrated in simplified form in FIG. 2. Generally, axons carryingimpulses from the cochlea connect to the inferior colliculus 201 and themedial geniculate body 202 in the thalamus to the auditory cortex 203.Specifically, primary axons in synaptic contact with the hair cells ofthe organ of Corti (106 in FIG. 1A) have their cell bodies in the spiralganglion 204 and enter the brainstem at the juncture of the pons andcerebellum. Here, each axon bifurcates and synapses in the dorsal andventral cochlear nuclei 205, 206 of the medulla. Second order axons fromthe dorsal and ventral cochlear nuclei 205, 206 may synapse in thesuperior olive 207 or may pass directly to the nucleus of the inferiorcolliculus 201 via the lateral leminiscus 208. These connections may bemade both ipsilaterally (not shown) and contralaterally.

The second pathway connected to by the auditory nerve is theextralemniscal pathway. This pathway is also known as the non-classical,nonspecific, polysensory, or diffuse auditory pathway, and is used forautonomous reactions to auditory stimuli. Moller and Rollins have foundevidence suggesting that this pathway may also be used for hearing inchildren. The extralemniscal pathway is phylogenetically older than thelemniscal system. Because it is used for autonomous reactions, it is afaster transmission path and is also non-tonotopic and non-linear. Cellsof the extralemniscal pathway fire in burst mode and have a slowspontaneous firing rate relative to the lemniscal pathway cells. Theauditory extralemniscal pathway makes connections with the somatosensorysystem at the dorsal cochlear nucleus and the inferior colliculus.Extralemniscal connections at the inferior colliculus occur at theexternal nucleus and the dorsal cortex. These ascending pathways thenconnect at all divisions of the medial geniculate bodies, the posteriorintralaminar complex, and suprageniculate nuclei at the level of thesuperior colliculus. Afferent dorsal column neurons connect with theextralemniscal pathway at the external nucleus and the dorsal cortex.Dorsal column neurons may also connect directly with other auditoryneurons such as, for example, those in the cochlear nucleus. Peripheralnerve bodies located in the dorsal root ganglia connect to the dorsalcolumn via axonal extensions that may ascend directly to the brain orbrain stem, or may connect to ascending pathways via synapticconnections in the spinal cord.

Connections from the somatosensory system to the auditory system havebeen explored in the past. Information from the different sensorymodalities (sight, hearing, touch, etc.) is known to integrate in mosthigher organisms, and occurs in the human nervous system. Co-existingcutaneous and auditory responses in neuronal tissue have been observedin the caudomedial auditory cortex, adjacent to the primary auditorycortex (Fu et al., Foxe et al.).

There are also connections between the trigeminal system and the ventralcochlear nucleus. The dorsal cochlear nucleus receives input from thedorsal column (proprioception) nuclei and the ventral cochlear nucleusfrom the trigeminal ganglion (Shore, Vass et al. 2000; Shore, El Kashlanet al. 2003; Weinberg and Rustioni 1987). The trigeminal ganglion alsoconnects to the superior olivary nucleus (Shore, Vass et al. 2000).Electrical stimulation of the somatosensory trigeminal ganglion caninfluence the activity of central auditory neurons in a manner distinctfrom acoustic stimulation, suggesting activation of non-classicalauditory pathways (El-Kashlan and Shore 2004). Furthermore, theactivation seems to be predominantly ipsilateral (El-Kashlan and Shore2004). These connections may be involved in generating or modulatingperceptions of phantom sounds which can be modified by manipulations ofsomatic regions of the head and neck (“somatic tinnitus”) (Levine, Abelet al. 2003; Shore, El Kashlan et al. 2003). Also, C2 (occipital andgreater auricular nerve) innervates the dorsal cochlear nucleus (Kanoldand Young 2001) as well as the rest of the body via the cuneate nucleusof the dorsal column (Itoh, Kamiya et al. 1987; Wright and Ryugo 1996).

Thus, it is envisioned that stimulation of the somatosensory system cantreat auditory dysfunction, for example, tinnitus by activation of theextralemniscal auditory connections to the somatosensory system.

III. Electrical Stimulation Devices

FIGS. 3A-3B illustrate example neurological stimulation systems 10 forelectrically stimulating a predetermined site, for example, a peripheralnerve, to treat auditory dysfunction. In general terms, stimulationsystem 10 includes an implantable electrical stimulation source 12 andone or more implantable electrical stimulation leads 14 for applyingelectrical stimulation pulses to a predetermined site. In operation, oneor both of these primary components are implanted in or on a subject'sbody, as discussed below. In certain embodiments, stimulation source 12is coupled directly to a connecting portion 16 of stimulation lead 14.In certain other embodiments, stimulation source 12 is incorporated intothe stimulation lead 14 and stimulation source 12 instead is embeddedwithin stimulation lead 14. For example, such a stimulation system 10may be a Bion® stimulation system manufactured by Advanced BionicsCorporation. Whether stimulation source 12 is coupled directly to orembedded within the stimulation lead 14, stimulation source 12 controlsthe stimulation pulses transmitted to one or more stimulation electrodes18 located on a stimulating portion 20 of stimulation lead 14,positioned in communication with a predetermined site, according tosuitable stimulation parameters (e.g., duration, amplitude or intensity,frequency, pulse width, etc.). One example of stimulation parametersused to treat an auditory dysfunction, such as, for example, tinnitususes an amplitude in the range of about 2 mA to about 100 mA, afrequency in the range of about 3 Hz to about 80 Hz, and a pulse widthin the range of about 5 microseconds to about 100 microseconds.

The predetermined site in communication with the stimulation lead 14 isa peripheral nerve in a preferred embodiment. Peripheral nerves caninclude cranial nerves for example, olfactory nerve, optic nerve,oculomotor nerve, trochlear nerve, trigeminal nerve, abducens nerve,facial nerve, vestibulocochlear (auditory) nerve, glossopharyngealnerve, vagal nerve, accessory nerve, and the hypoglossal nerve. Inaddition to cranial nerves, the predetermined site can be a dermatomearea, for example, C2, C3, C4, C5, C6, C7, C8, as well as any thoracic,lumbar or sacral dermatome. Other dermatomes that can be included in thepresent invention include dermatomes associated with cranial nerveshaving somatosensory function, for example, but not limited todermatomes associated with the trigeminal nerve, intermediate part ofthe facial nerve, glossopharyngeal nerve, or vagal nerve. Peripheralnerves also includes spinal nerves, which in general, spinal nerves arenamed after the vertebral segment of the spinal column above theirorigin. For example, the spinal nerve originating under the thirdthoracic vertebra may be termed the third thoracic nerve. Thus, spinalnerves can include, but are limited to cervical nerve roots (e.g., C1,C2, C3, C4, C5, C6, C7 and C8), thoracic nerve roots (e.g., T1, T2, T3,T4, T5, T6, T7, T8, T9, T10, T11, T12), lumbar nerve roots (L1, L2, L3,L4, L5) sacral nerve roots (e.g., S1, S2, S3, S4, S5) and the coccygealnerve. Other peripheral nerves are spinal nerves such as thesuboccipital nerve, the greater occipital nerve, the lesser occipitalnerve, the greater auricular nerve, the lesser auricular nerve, thephrenic nerve, and the brachial plexus, which branches to form thedorsal scapular nerve, the thoracic nerve, the suprascapular nerve, thelateral pectoral, the musculocutaneous nerve, the axillarily nerve, theradial nerve, the median nerve, the ulnar nerve, the intercostal nerves,and other minor peripheral nerves, as well as parasympathetic and/orsympathetic nerves. In certain embodiments, the peripheral nervestimulated is the trigeminal nerve or the trigeminal dermatome or anyperipheral nerve associated with the C2 dermatome area, C3 dermatomearea, cranial nerves, the median nerve or any combination thereof.Peripheral nerve ganglia, which are collections of peripheral nerve cellbodies, are predetermined sites in communication with stimulation lead14 in certain embodiments. A doctor, the patient, or another user ofstimulation source 12 may directly or indirectly input stimulationparameters to specify or modify the nature of the stimulation provided.In certain embodiments, transcutaneous implantation of stimulation lead14 is used either permanently or temporarily.

Some embodiments employ a burst stimulus. Examples of burst stimulus arefound in U.S. Application entitled “New Stimulation Design forNeuromodulation”, filed Oct. 20, 2005, and incorporated herein byreference. The burst stimulus comprises a frequency in the range ofabout 1 Hz to about 300 Hz, more particular, in the range of about 1 Hzto about 12 Hz, and more particularly, in the range of about 1 Hz toabout 4 Hz, 4 Hz to about 7 Hz or about 8 Hz to about 12 Hz, 18 Hz to 20Hz, and 40 Hz. The burst stimulus comprises at least two spikes, forexample, each burst stimulus can comprise about 12 to about 100 spikes,more particularly, about 2 to about 10 spikes. Each spike can comprise afrequency in the range of about 50 Hz to about 1000 Hz, moreparticularly, in the range of about 200 Hz to about 500 Hz. The intervalbetween spikes can be about 0.5 milliseconds to about 100 milliseconds.The frequency of the spikes within the burst does not need to beconstant or regular, in fact, typically, the frequency of the spikes israndom or variable. In further embodiments, the burst stimulus isfollowed by an inter-burst interval. The inter-burst interval has aduration in the range of about 5 milliseconds to about 5 seconds, morepreferably, about 10 milliseconds to about 300 milliseconds, or anyrange therebetween. It is envisioned that the burst stimulus has aduration in the range of about 10 milliseconds to about 5 seconds, moreparticularly in the range of about 250 milliseconds to 1second. Theburst stimulus and the inter-burst interval can have a regular patternor an irregular pattern (e.g., random or irregular harmonics).

In one embodiment, as shown in FIG. 3A, stimulation source 12 includesan implantable pulse generator (IPG). An exemplary IPG may be oneincorporated in the Genesis® System manufactured by AdvancedNeuromodulation Systems, Inc., part numbers 3604, 3608, 3609, and 3644.In another embodiment, as shown in FIG. 3B, stimulation source 12includes an implantable wireless receiver. An example wireless receivermay be one incorporated in the Renew® System manufactured by AdvancedNeuromodulation Systems, Inc., part numbers 3408 and 3416. The wirelessreceiver is capable of receiving wireless signals from a wirelesstransmitter 22 located external to the person's body. In someembodiments, the receiver may be stand-alone and no external controller26 is required. The wireless signals are represented in FIG. 3B bywireless link symbol 24. A doctor, the patient, or another user ofstimulation source 12 may use a controller 26 located external to theperson's body to provide control signals for operation of stimulationsource 12. Controller 26 provides the control signals to wirelesstransmitter 22, wireless transmitter 22 transmits the control signalsand power to the wireless receiver of stimulation source 12, andstimulation source 12 uses the control signals to vary the stimulationparameters of stimulation pulses transmitted through stimulation lead 14to the predetermined peripheral nerve. Thus, the external controller 26can be for example, a handheld programmer, to provide a means forprogramming the IPG. An example wireless transmitter 122 may be onemanufactured by Advanced Neuromodulation Systems, Inc., such as theRenew® System, part numbers 3508 and 3516.

Conventional neuromodulation devices can be modified to apply burststimulation to nerve tissue of a patient by modifying the softwareinstructions stored in the devices. Specifically, conventionalneuromodulation devices typically include a microprocessor and a pulsegeneration module. The pulse generation module generates the electricalpulses according to a defined pulse width and pulse amplitude andapplies the electrical pulses to defined electrodes. The microprocessorcontrols the operations of the pulse generation module according tosoftware instructions stored in the device.

These conventional neuromodulation devices can be adapted by programmingthe microprocessor to deliver a number of spikes (relatively short pulsewidth pulses) that are separated by an appropriate inter-spike interval.Thereafter, the programming of the microprocessor causes the pulsegeneration module to cease pulse generation operations for aninter-burst interval. The programming of the microprocessor also causesa repetition of the spike generation and cessation of operations for apredetermined number of times. After the predetermined number ofrepetitions have been completed, the microprocessor can cause burststimulation to cease for an amount of time (and resume thereafter).Also, in some embodiments, the microprocessor could be programmed tocause the pulse generation module to deliver a hyperpolarizing pulsebefore the first spike of each group of multiple spikes.

The microprocessor can be programmed to allow the variouscharacteristics of the burst stimulus to be set by a physician to allowthe burst stimulus to be optimized for a particular pathology of apatient. For example, the spike amplitude, the inter-spike interval, theinter-burst interval, the number of bursts to be repeated in succession,the amplitude of the hyperpolarizing pulse, and other suchcharacteristics could be controlled using respective parameters accessedby the microprocessor during burst stimulus operations. These parameterscould be set to desired values by an external programming device viawireless communication with the implantable neuromodulation device.

In another embodiment, a neuromodulation device can be implemented toapply burst stimulation using a digital signal processor and one orseveral digital-to-analog converters. The burst stimulus waveform couldbe defined in memory and applied to the digital-to-analog converter(s)for application through electrodes of the medical lead. The digitalsignal processor could scale the various portions of the waveform inamplitude and within the time domain (e.g., for the various intervals)according to the various burst parameters.

FIGS. 4A-4I illustrate example stimulation leads 14 that may be used forelectrically stimulating a predetermined peripheral nerve for treatingauditory dysfunction. As described above, each of the one or morestimulation leads 14 incorporated in stimulation system 10 includes oneor more stimulation electrodes 18 adapted to be positioned incommunication with the predetermined peripheral nerve and used todeliver to the stimulation pulses received from stimulation source 12. Apercutaneous stimulation lead 14, such as example stimulation leads 14a-d, includes one or more circumferential electrodes 18 spaced apartfrom one another along the length of stimulating portion 20 ofstimulation lead 14. Circumferential electrodes 18 emit electricalstimulation energy generally radially (i.e., generally perpendicular tothe axis of stimulation lead 14) in all directions. A laminotomy,paddle, or surgical stimulation lead 14, such as example stimulationleads 14 e-i, includes one or more directional stimulation electrodes 18spaced apart from one another along one surface of stimulation lead 14.Directional stimulation electrodes 18 emit electrical stimulation energyin a direction generally perpendicular to the surface of stimulationlead 14 on which they are located. Although various types of stimulationleads 14 are shown as examples, the present invention contemplatesstimulation system 10 including any suitable type of stimulation lead 14in any suitable number. In addition, stimulation leads 14 may be usedalone or in combination. For example, unilateral stimulation of aperipheral nerve may be accomplished using a single electricalstimulation lead 14 implanted in communication with the nerve on oneside of the subject's body, while bilateral electrical stimulation ofthe peripheral nerve may be accomplished using two stimulation leads 14implanted in communication with the peripheral nerve on both sides ofthe subject's body. Multi-nerve implantation of stimulation leads can beused.

In one embodiment, the stimulation source is transcutaneously incommunication with the electrical stimulation lead. In “transcutaneous”,electrical nerve stimulation (TENS) the stimulation source is externalto the patient's body, and may be worn in an appropriate fanny pack orbelt, and the electrical stimulation lead is in communication with thestimulation source, either remotely or directly. In another embodiment,the stimulation is percutaneous. In “percutaneous” electrical nervestimulation (PENS), needles are inserted to an appropriate depth aroundor immediately adjacent to a predetermined stimulation site, and thenstimulated.

In addition to electrical stimulation, other forms of stimulation can beused, for example magnetic. Magnetic stimulation can be provided byinternally implanted probes or by externally applied directed magneticfields, for example, U.S. Pat. Nos. 6,592,509; 6,132,361; 5,752,911; and6,425,852, each of which is incorporated herein in its entirety. Quickpulses of magnetic stimulation can be applied externally ortranscranially, for example repetitive transcranially magneticstimulation (rTMS).

Whether using percutaneous leads, laminotomy leads, or some combinationof both, the leads are coupled to one or more conventionalneurostimulation devices, or signal generators. The devices can betotally implanted systems and/or radio frequency (RF) systems. Anexample of an RF system is a MNT/MNR-916CC system manufactured byAdvanced Neuromodulation Systems, Inc.

The preferred neurostimulation devices should allow each electrode ofeach lead to be defined as a positive, a negative, or a neutralpolarity. For each electrode combination (e.g., the defined polarity ofat least two electrodes having at least one cathode and at least oneanode), an electrical signal can have at least a definable amplitude(e.g., voltage), pulse width, and frequency, where these variables maybe independently adjusted to finely select the sensory transmittingnerve tissue required to inhibit transmission of neuronal signals.Generally, amplitudes, pulse widths, and frequencies are determinable bythe capabilities of the neurostimulation systems, which are known bythose of skill in the art. Voltages that may be used can include, forexample about 0.5 to about 10 volts, more preferably about 1 to about 10volts.

It is envisaged that the patient will require intermittent assessmentwith regard to patterns of stimulation. Different electrodes on the leadcan be selected by suitable computer programming, such as that describedin U.S. Pat. No. 5,938,690, which is incorporated by reference here infull. Utilizing such a program allows an optimal stimulation pattern tobe obtained at minimal voltages. This ensures a longer battery life forthe implanted systems.

IV. Implantation of Electrical Devices

FIG. 5 illustrates example placement of a single stimulation lead 14 formedial electrical stimulation of a peripheral nerve dorsal root gangliaby a stimulation electrode 18. Those of skill in the art are aware thatthe peripheral nerves can be stimulated anywhere along the nerve. Thus,it is not necessary to stimulate the dorsal root ganglia. Multiplestimulation leads 14 and electrodes 18 are used in other embodiments ofthe invention.

FIG. 6 is an illustration of an implantable pulse generator with asingle simulation lead 14 that is employed with two stimulationelectrodes 18 for bilateral stimulation of peripheral nerve dorsal rootganglia 20. As indicated above, those of skill in the art realize thatthe peripheral nerve can be stimulated anywhere along the nerve.

FIG. 4 illustrate examples of one or more stimulation leads 14 implantedsubcutaneously such that one or more stimulation electrodes 18 of eachstimulation lead 14 are positioned in communication with the a dermatome(e.g., C2-C8, T1-T12, L1-L5, S1-S5), cervical nerve roots (e.g., C1, C2,C3, C4, C5, C6, C7 and C8) cranial nerves (e.g., olfactory nerve, optic,nerve, oculomoter nerve, trochlear nerve, trigeminal nerve, abducentnerve, facial nerve, vestibulocochlear nerve, glossopharyngeal nerve,vagal nerve, accessory nerve, and hypoglossal nerve), thoracic nerveroots (e.g., T1, T2, T3, T4, T5, T6, T7, T8, T9, T10, T11, T12), lumbarnerve roots (e.g., L1, L2, L3, L4, L5), sacral nerve roots (S1, S2, S3,S4, S5), as well as any other spinal or peripheral nerve. Otherdermatomes that can be included in the present invention includedermatomes associated with cranial nerves having somatosensory function,for example, but not limited to dermatomes associated with thetrigeminal nerve, intermediate part of the facial nerve,glossopharyngeal nerve, or vagal nerve. FIGS. 7 and 8 illustrate exampleplacement of a single stimulation lead 14 for medial electricalstimulation of a dermatome area. FIG. 8 illustrates example placement ofan electrode in the occipital area or C2/C3 dermatome area. In certainembodiments one or more stimulation electrodes 18 are positioned in theC2 dermatome area, subcutaneously, but superior to the galea. Withincertain areas of the C2 dermatome area, there is little or no muscle,this area primarily consists of fat, fascia, periostium, andneurovascular structures (e.g., galea). Thus, the advantage implanting astimulation lead in this area is that there will be no to littlemuscular contraction. One of skill in the art is aware that stimulationof the C2 dermatome area may result in stimulation of various neuronalstructures, for example, but not limited to the C2 dermatome area, C3dermatome, trigeminal dermatome, trigeminal nerve, olfactory nerve,other cranial nerves, or other cervical nerve roots.

Different numbers of stimulation leads 14 and stimulation electrodes 18may be used in other embodiments of the invention. Additionally, otherperipheral nerves or peripheral nerve branches are stimulated bystimulation electrodes 18 in certain embodiments.

FIG. 9 illustrates an example method of treating auditory dysfunctionusing stimulation system 10, described above, implanted into a person'sbody with stimulation lead 14 located in communication with a peripheralnerve for treating auditory dysfunction. At process 800, one or morestimulation leads 14 are implanted such that one or more stimulationelectrodes 18 of each stimulation lead 14 are positioned incommunication with a peripheral nerve (for the purposes described hereinand as those skilled in the art will recognize, when an embeddedstimulation system, such as the Bion®, is used, it is positioned similarto positioning the lead 14). Techniques for implanting stimulation leadssuch as stimulation lead 14 are known to those skilled in the art. Incertain embodiments, as described above, one or more stimulationelectrodes 18 are positioned in communication with a peripheral nerve.Stimulation electrodes 18 are commonly positioned in communication withthe peripheral nerve by electrodes applied cutaneously to the dermatomearea of a peripheral nerve. Stimulation electrodes 18 can also bepositioned subcutaneously in communication with the peripheral nerve oron the nerve root ganglion. The electrodes are carried by two primaryvehicles: percutaneous leads and a laminotomy lead. Percutaneous leadscommonly have two or more, equally-spaced electrodes, which are placedsubcutaneously in communication with the peripheral nerve. Forunilateral auditory dysfunction, percutaneous leads are positioned onthe peripheral nerve on the contralateral side of the body correspondingto the “afflicted” side of the body, and for bilateral auditorydysfunction, a single percutaneous lead with two or more leads ispositioned with each lead in communication with a peripheral nerve. Anexample of an eight-electrode percutaneous lead is an OCTRODE® leadmanufactured by Advanced Neuromodulation Systems, Inc. Use of a Bion®stimulation system manufactured by Advanced Bionics Corporation is alsocontemplated in certain embodiments.

In contrast to the percutaneous leads, laminotomy leads have a paddleconfiguration and typically possess a plurality of electrodes (forexample, two, four, eight, or sixteen) arranged in one or more columns.An example of a sixteen-electrode laminotomy lead is shown in FIG. 4H.Another example of a laminotomy lead is an eight-electrode, two columnlaminotomy lead called the LAMITRODE® 44, which is manufactured byAdvanced Neuromodulation Systems, Inc. Implanted laminotomy leads arecommonly transversely centered over the physiological midline of apatient. In such position, multiple columns of electrodes are wellsuited to address bilateral auditory dysfunction, where electricalenergy may be administered bilaterally near peripheral nerve gangliaaround the spinal cord via a single laminotomy lead. A multi-columnlaminotomy lead enables reliable positioning of a plurality ofelectrodes, and in particular, a plurality of electrode columns that donot readily deviate from an initial implantation position.

Laminotomy leads require a surgical procedure for implantation. Thesurgical procedure, or partial laminectomy, requires the resection andremoval of certain vertebral tissue to properly position the laminotomylead. The laminotomy lead offers a more stable platform, which isfurther capable of being sutured in place, that tends to migrate less inthe operating environment of the human body. Depending on the positionof insertion, however, access to the peripheral nerve or nerve gangliamay only require a partial removal of the ligamentum flavum at theinsertion site. In some embodiments, two or more laminotomy leads may bepositioned to treat multiple peripheral nerves or multiple branch pointsof a single nerve.

In addition to stimulation of peripheral nerve ganglia, the laminotomyor percutaneous leads can be implanted subcutaneously in the dermatomearea as shown in FIGS. 7 and 8 to stimulate any cranial and/or cervicalnerve root associated with the C2 dermatome area. The leads can also beimplanted subcutaneously at other dermatomes such as C3, trigeminalnerve dermatome, etc.

At process 802, if necessary, stimulation source 12 may be coupleddirectly to connecting portion 16 of stimulation lead 14. Alternatively,as described above and if necessary, stimulation source 12 may not becoupled directly to stimulation lead 14 and may instead be coupled tostimulation lead 14 via an appropriate wireless link. Of course, asthose skilled in the art know, an embedded stimulation system will notneed to be so coupled.

Intra-implantation trial stimulation may be conducted at processes 804through 808. These processes may be used to optimize the effect of thetreatment on auditory dysfunction. In certain embodiments, theintra-implantation trial stimulation is not performed, and the methodproceeds from process 802 to 810. At process 804, stimulation source 12is activated to generate and transmit stimulation pulses via one or morestimulation electrodes 18. At process 806, informal subjectivequestioning of the person, formal subjective testing and analysisaccording to one or more audiology tests and/or other analyses (such asthe Goebel tinnitus questionnaire or other validated tinnitusquestionnaires, audiometry, tinnitus matching, impedence, BAEP, and OAE)may be performed to determine whether the subject's auditory dysfunctionhas sufficiently improved through the intra-implantation trialstimulation. If the subject's auditory dysfunction has not sufficientlyimproved, one or more stimulation parameters may be adjusted,stimulation lead 14 may be moved incrementally or even re-implanted, orboth of these modifications may be made at process 808 and the trialstimulation and analysis repeated until the auditory dysfunction hassufficiently improved. Once the stimulation parameters have beenproperly set and stimulation lead 14 has been properly positioned suchthat subject's auditory dysfunction has improved, intra-implantationtrial stimulation is complete. One of skill in the art is aware thatother types of intra-implantation trailing methods or stimulation trailscan be used in the present invention, for example, but not limited totranscutaneous electrical nerve stimulation (TENS), transmagneticstimulation (TMS), nerve blocks, etc.

Once stimulation lead 14 has been properly implanted and secured, andany trial stimulation completed, if necessary, stimulation source 12 isimplanted at process 810. Techniques for implanting stimulation sourcessuch as stimulation source 12 are known to those skilled in the art. Fornon-embedded systems, the implant site is typically a subcutaneouspocket formed to receive and house stimulation source 12. The implantsite is usually located some distance away from the insertion site, suchas in or near the lower back or buttocks. Where stimulation lead 14includes connecting portion 16, connecting portion 16 may be tunneled,at least in part, subcutaneously to the implant site of stimulationsource 12 at process 812. Some embodiments of the invention may use anon-implantable stimulation source. At process 814, a doctor, thepatient, or another user of stimulation source 12 may directly orindirectly input stimulation parameters for controlling the nature ofthe electrical stimulation provided to the peripheral nerve, if notalready set during any intra-implantation trial stimulation period.Where appropriate, post-implantation trial stimulation may be conducted,over one or more weeks or months for example, and any necessarymodifications made accordingly.

Although example processes are illustrated and described, the presentinvention contemplates two or more processes taking place substantiallysimultaneously or in a different order. In addition, the presentinvention contemplates using methods with additional processes, fewerprocesses, or different processes, so long as the processes remainappropriate for implanting stimulation system 10 into a person forelectrical stimulation of the predetermined site, such as, for examplethe C2 dermatome area, C3 dermatome area, a cervical (e.g., C1, C2, C3,etc) or other spinal nerve or any cranial nerve (e.g., trigeminal,olfactory, etc) to treat auditory dysfunction.

One technique that offers the ability to affect neuronal function is thedelivery of electrical stimulation for neuromodulation directly totarget tissues via an implanted device having a probe. The probe is astimulation lead or electrode in certain embodiments. The electrodeassembly may be one electrode, multiple electrodes, or an array ofelectrodes in or around the target area. The proximal end of the probeis coupled to system to operate the device to stimulate the target site.Thus, the probe is coupled to an electrical signal source which, inturn, is operated to stimulate the predetermined treatment site.

V. Infusion Pumps

In further embodiments, it may be desirable to use a drug deliverysystem independently or in combination with electrical stimulation toresult in the stimulation parameters of the present invention. Drugdelivery may be used independent of or in combination with alead/electrode to provide electrical stimulation and chemicalstimulation. When used, the drug delivery catheter is implanted suchthat the proximal end of the catheter is coupled to a pump and adischarge portion for infusing a dosage of a pharmaceutical or drug.Implantation of the catheter can be achieved by combining data from anumber of sources including CT, MRI or conventional and/or magneticresonance angiography into the stereotactic targeting model. Thus,implantation of the catheter can be achieved using similar techniques asdiscussed above for implantation of electrical leads, which isincorporated herein. The distal portion of the catheter can havemultiple orifices to maximize delivery of the pharmaceutical whileminimizing mechanical occlusion. The proximal portion of the cathetercan be connected directly to a pump or via a metal, plastic, or otherhollow connector, to an extending catheter.

Implantable infusion pumps are used with certain embodiments of theinvention to provide chemical stimulation. Further details ofimplantable infusion pumps that may be used with the invention are foundin pending U.S. application Ser. No. 10/755,985 “Actuation System andMethod for an Implantable Infusion Pump” herein incorporated byreference.

In further embodiments, “active pumping” devices or so-calledperistaltic pumps can be used as described in U.S. Pat. Nos. 4,692,147,5,840,069, and 6,036,459, which are incorporated herein by reference intheir entirety. Peristaltic pumps are used to provide a metered amountof a drug in response to an electronic pulse generated by controlcircuitry associated within the device. An example of a commerciallyavailable peristaltic pump is SynchroMed® implantable pump fromMedtronic, Inc., Minneapolis, Minn.

Other pumps that may be used in the present invention includeaccumulator-type pumps, for example certain external infusion pumps fromMinimed, Inc., Northridge, Calif. and Infusaid® implantable pump fromStrato/Infusaid, Inc., Norwood, Mass. Passive pumping mechanisms can beused to release an agent in a constant flow or intermittently or in abolus release. Passive type pumps include, for example, but are notlimited to gas-driven pumps described in U.S. Pat. Nos. 3,731,681 and3,951,147; and drive-spring diaphragm pumps described in U.S. Pat. Nos.4,772,263, 6,666,845, 6,620,151 all of which are incorporated byreference in their entirety. Pumps of this type are commerciallyavailable, for example, Model 3000® from Arrow International, Reading,Pa. and IsoMed® from Medtronic, Inc., Minneapolis, Minn.; AccuRx® pumpfrom Advanced Neuromodulation Systems, Inc., Plano, Tex.

Instances in which chemical and electrical stimulation will beadministered to the subject, a catheter having electrical leads may beused, similar to the ones described in U.S. Pat. Nos. 6,176,242;5,423,877; 5,458,631 and 5,119,832, each of which are incorporatedherein by reference in its entirety.

Still further, the present invention can comprise a chemical stimulationsystem that comprises a system to control release of neurotransmitters(e.g., glutamate, acetylcholine, norepinephrine, epinephrine), chemicals(e.g., zinc, magnesium, lithium) and/or pharmaceuticals that are knownto alter the activity of neuronal tissue. For example, infusionformulation delivery system can utilize a control system having aninput-response relationship. A sensor generates a sensor signalrepresentative of a system parameter input (such as levels ofneurotransmitters), and provides the sensor signal to a controller. Thecontroller receives the sensor signal and generates commands that arecommunicated to the infusion formulation delivery device. The infusionformulation delivery device then delivers the infusion formulationoutput to the predetermined site at a determined rate and amount inorder to control the system parameter.

Sensor may comprise a sensor, sensor electrical components for providingpower to the sensor and generating the sensor signal, a sensorcommunication system for carrying the sensor signal to controller, and asensor housing for enclosing the electrical components and thecommunication system. Controller may include one or more programmableprocessors, logic circuits, or other hardware, firmware or softwarecomponents configured for implementing the control functions describedherein, a controller communication system for receiving the sensorsignal from the sensor, and a controller housing for enclosing thecontroller communication system and the one or more programmableprocessors, logic circuits, or other hardware, firmware or softwarecomponents. The infusion formulation delivery device may include asuitable infusion pump, infusion pump electrical components for poweringand activating the infusion pump, an infusion pump communication systemfor receiving commands from the controller, and an infusion pump housingfor enclosing the infusion pump, infusion pump electrical components,and infusion pump communication system. Such systems are described inU.S. Pat. No. 6,740,072, which is incorporated herein by reference inits entirety.

In certain embodiments, the sensor can be an electrode that senses ahyperactive burst pattern of activity, which in turns stimulates theinfusion pump to release a chemical or stimulating drug or agent tomodify the neuronal activity. The chemical or stimulating agent can beeither an inhibiting agent or stimulating agent.

Herein, stimulating drugs comprise medications, anesthetic agents,synthetic or natural peptides or hormones, neurotransmitters, cytokinesand other intracellular and intercellular chemical signals andmessengers, other agents such as zinc and the like. In addition, certainneurotransmitters, hormones, and other drugs are excitatory for sometissues, yet are inhibitory to other tissues. Therefore, where, herein,a drug is referred to as an “excitatory” drug, this means that the drugis acting in an excitatory manner, although it may act in an inhibitorymanner in other circumstances and/or locations. Similarly, where an“inhibitory” drug is mentioned, this drug is acting in an inhibitorymanner, although in other circumstances and/or locations, it may be an“excitatory” drug. In addition, stimulation of an area herein includesstimulation of cell bodies and axons in the area.

Similarly, excitatory neurotransmitter agonists (e.g., norepinephrine,epinephrine, glutamate, acetylcholine, serotonin, dopamine), agoniststhereof, and agents that act to increase levels of an excitatoryneurotransmitter(s) (e.g., edrophonium; Mestinon; trazodone; SSRIs(e.g., flouxetine, paroxetine, sertraline, citalopram and fluvoxamine);tricyclic antidepressants (e.g., imipramine, amitriptyline, doxepin,desipramine, trimipramine and nortriptyline), monoamine oxidaseinhibitors (e.g., phenelzine, tranylcypromine, isocarboxasid)),generally have an excitatory effect on neural tissue, while inhibitoryneurotransmitters (e.g., dopamine, glycine, and gamma-aminobutyric acid(GABA)), agonists thereof, and agents that act to increase levels of aninhibitory neurotransmitter(s) generally have an inhibitory effect(e.g., benzodiasepine (e.g., chlordiazepoxide, clonazepam, diazepam,lorazepam, oxazepam, prazepam alprazolam); flurazepam, temazepam, ortriazolam). (Dopamine acts as an excitatory neurotransmitter in somelocations and circumstances, and as an inhibitory neurotransmitter inother locations and circumstances.) However, antagonists of inhibitoryneurotransmitters (e.g., bicuculline) and agents that act to decreaselevels of an inhibitory neurotransmitter(s) have been demonstrated toexcite neural tissue, leading to increased neural activity. Similarly,excitatory neurotransmitter antagonists (e.g., prazosin, and metoprolol)and agents that decrease levels of excitatory neurotransmitters mayinhibit neural activity. Yet further, lithium salts, anesthetics (e.g.,lidocane), and magnesium may also be used in combination with electricalstimulation.

VI. Treatment of Auditory Dysfunction

The present method acts to stimulate nerve afferents which in turnstimulate the brain and cause/allow the brain to act in the bestinterest of the host through use of the brain's natural mechanisms. Theprior art fails to recognize that stimulation of a patient's peripheralnerves can provide the therapeutic treatments for auditory dysfunctionaccording to the instant invention.

The present invention is particularly useful in the treatment ofauditory dysfunction in humans. However, one skilled in the artappreciates that the present invention is applicable to other animalswhich experience auditory dysfunction. This may include, for example,primates, canines, felines, horses, elephants, dolphins, etc. Utilizingthe various embodiments of the present invention, one skilled in the artmay be able to modulate the auditory system via peripheral nervestimulation to achieve a desirable result.

One technique that offers the ability to affect neuronal function is thedelivery of electrical, chemical, and/or magnetic stimulation forneuromodulation directly to target tissues via an implanted devicehaving a probe. The probe is, for example, a stimulation lead, electrodeassembly, or a catheter in certain embodiments of the invention. Anelectrode assembly may be one electrode, multiple electrodes, or anarray of electrodes in or around the target area. The proximal end ofthe probe is coupled to system to operate the device to stimulate thetarget site. Thus, the probe is coupled to an electrical signal source,which, in turn, is operated to stimulate the predetermined treatmentsite of a peripheral nerve or nerves. In the case of unilateral auditorydysfunction, contralateral peripheral nerve stimulation may be moreeffective than ipsilateral stimulation. However, as the auditory systemcrosses over at numerous points, effective auditory dysfunctiontreatment may require bilateral stimulation. Stimulation of thepredetermined site is performed to modulate neuronal extralemniscalpathways of the auditory system. Modulation of this neuronal tissue mayresult in efficacious treatment of auditory dysfunction in a subject.While optimal results from the treatment may result in the completecessation of auditory dysfunction in a subject, any lessening of theamplitude of a subject's auditory dysfunction may be consideredsuccessful according to the present invention.

The predetermined site can be, for example, but not limited to adermatome area, for example, C2, C3, C4, C5, C6, C7, C8, as well as anythoracic, lumbar or sacral dermatome. Cervical nerve roots (e.g., C1,C2, C3, C4, C5, C6, C7 and C8) and cranial nerves (e.g., olfactorynerve, optic, nerve, oculomoter nerve, trochlear nerve, trigeminalnerve, abducent nerve, facial nerve, vestibulocochlear nerve,glossopharyngeal nerve, vagal nerve, accessory nerve, and hypoglossalnerve) to provide therapeutic treatments according to the instantinvention. Other dermatomes that can be included in the presentinvention include dermatomes associated with cranial nerves havingsomatosensory function, for example, but not limited to dermatomesassociated with the trigeminal nerve, intermediate part of the facialnerve, glossopharyngeal nerve, or vagal nerve. Other peripheral nervesare spinal nerves such as the suboccipital nerve, the greater occipitalnerve, the lesser occipital nerve, the greater auricular nerve, thelesser auricular nerve, the phrenic nerve, and the brachial plexus,which branches to form the dorsal scapular nerve, the thoracic nerve,the suprascapular nerve, the lateral pectoral, the musculocutaneousnerve, the axillarily nerve, the radial nerve, the median nerve, theulnar nerve, and other minor peripheral nerves, as well as sympatheticand parasympathetic nerves. Yet further, other peripheral nerves alsoincludes thoracic nerve roots (e.g., T1, T2, T3, T4, T5, T6, T7, T8, T9,T10, T11, T12), lumbar nerve roots (L1, L2, L3, L4, L5) sacral nerveroots (e.g., S1, S2, S3, S4, S5) and the coccygeal nerve.

One example of stimulation parameters that can be used in the presentinvention is a parameter set with an amplitude in the range of about 2mA to about 100 mA, a frequency in the range of about 1 Hz to about 80Hz, and a pulse width in the range of about 5 microseconds to about 100microseconds.

One of skill in the art is aware that stimulation parameters can bevaried to achieve the desired result. One such parameter that may bevaried in the present invention is signal frequency. Altering thefrequency signal can result in the generation of a bursting type rhythmor burst stimulus frequency or burst mode stimulation, as described in“New Stimulation Design for Neuromodulation”, filed Oct. 20, 2005incorporated by reference herein.

In certain embodiments, the burst stimulus frequency may be in the rangeof about 1 Hz to about 100 Hz, more particular, in the range of about 1Hz to about 12 Hz, and more particularly, in the range of about 1 Hz toabout 4 Hz, 4 Hz to about 7 Hz or about 8 Hz to about 12 Hz for eachburst. One skilled in the art will further realize that each burststimulus comprises at least one two spikes, for example, each burststimulus can comprise about 2 to about 100 spikes, more particularly,about 2 to about 10 spikes. Each spike can comprise a frequency in therange of about 50 Hz to about 1000 Hz, more particularly, in the rangeof about 200 Hz to about 500 Hz. One of skill in the art is aware thatthe frequency for each spike within a burst can be variable, thus it isnot necessary for each spike to contain similar frequencies, e.g., thefrequencies can vary in each spike. The inter-spike interval can be alsovary, for example, the inter-spike interval, can be about 0.5milliseconds to about 100 milliseconds or any range therebetween. Theburst stimulus is followed by an inter-burst interval a duration in therange of about 5 milliseconds to about 5 seconds, preferably, about 10milliseconds to about 300 milliseconds. It is envisioned that the burststimulus has a duration in the range of about 10 milliseconds to about 5seconds, more particular, in the range of about 250 msec to 1000 msec(1-4 Hz burst firing), 145 msec to about 250 msec (4-7 Hz,), 145 msec toabout 80 msec (8-12 Hz) or 1 to 5 seconds in plateau potential firing.The burst stimulus and the inter-burst interval can have a regularpattern or an irregular pattern (e.g., random or irregular harmonics).

In the auditory system, tonic firing the contents of auditoryinformation, while burst firing may transmit the change in the auditoryenvironment and valence or importance attached to that sound (Lisman1997; Sherman 2001; Swadlow and Gusev 2001). Repetitive stimuluspresentation results in decreased neuronal response to that stimulus,known as auditory habituation at the single cell level (Ulanovsky etal., 2003), auditory mismatch negativity at multiple cell level(Naatanen et al., 1993; Ulanovsky et al., 2003).

Many auditory dysfunctions are constantly present. For example, tinnitusis usually constantly present, e.g., a non-rational valence is attachedto the internally generated sound, and there is no auditory habituationto this specific sound, at this specific frequency. Thus, tinnitus isthe result of hyperactivity of lesion-edge frequencies, and auditorymismatch negativity in tinnitus patients is specific for frequencieslocated at the audiometrically normal lesion edge (Weisz 2004).

As pathological valence of the tinnitus sound is mediated by burstfiring, burst firing is increased in tinnitus in the extralemniscalsystem (Chen and Jastreboff 1995; Eggermont and Kenmochi 1998; Eggermont2003), in the inner hair cells (Puel 1995; Puel et al., 2002), theauditory nerve (Moller 1984), the dorsal and external inferiorcolliculus (Chen and Jastreboff 1995), the thalamus (Jeanmonod, Magninet al., 1996) and the secondary auditory cortex (Eggermont and Kenmochi1998; Eggermont 2003). Furthermore, quinine, known to generate tinnitus,induces an increased regularity in burst firing, at the level of theauditory cortex, inferior colliculus and frontal cortex (Gopal and Gross2004). It is contemplated that tinnitus can only become conscious if anincreased tonic firing rate is present in the lemniscal system,generating the sound. This increased firing activity has beendemonstrated in the lemniscal dorsal cochlear nucleus (Kaltenbach,Godfrey et al., 1998; Zhang and Kaltenbach 1998; Kaltenbach and Afman2000; Brozoski, Bauer et al., 2002; Zacharek et al., 2002; Kaltenbach etal., 2004), inferior colliculus (Jastreboff and Sasaki 1986; Jastreboff,Brennan et al., 1988; Jastreboff 1990) (Gerken 1996) and primaryauditory cortex (Komiya, 2000). Interestingly, not only tonic firing isincreased generating the tinnitus sound, but also the burst firing (Ochiand Eggermont 1997) (keeping it conscious) at a regular basis.Repetitive burst firing is known to generate tonic gamma band activity(Gray and Singer 1989; Brumberg, 2000). Thus, it is envisioned that thepresent invention can be used to modify burst firing, thus modifyingtonic gamma activity. However, other pathways may be employed byembodiments of the invention that potentially contribute to thetreatment efficacy.

Burst mode firing boosts the gain of neural signaling of important ornovel events by enhancing transmitter release and enhancing dendriticdepolarization, thereby increasing synaptic potentiation. Conversely,single spiking mode may be used to dampen neuronal signaling and may beassociated with habituation to unimportant events (Cooper 2002). It isbelieved that the main problem in tinnitus is that the internallygenerated stimulus does not decay due to the presence of regularbursting activity telling the cortex this signal is important and has toremain conscious.

Thus, in the present invention, it is envisioned that a burst mode typestimulation can attack either of these two pathways: slowing down tonicfiring in the lemniscal system (below 40 Hz) or removing the valenceattached to it by the extralemniscal system by suppressing the burstingrhythm, thereby treating auditory dysfunctions such as tinnitus. Yetfurther, the system of the present invention can also make the auditorydysfunction disappear via auditory habituation. Suppressing the burstfiring in the frontal cortex may alter the emotional effect of tinnitus,with the tinnitus persisting, but without much influence on the dailylife of a tinnitus sufferer.

Thus, using the therapeutic stimulation system of the present invention,the predetermined site is stimulated in an effective amount or effectivetreatment regimen to decrease, reduce, modulate or abrogate theneurological disorder. Thus, a subject is administered a therapeuticallyeffective stimulation so that the subject has an improvement in theparameters relating to tinnitus including the Goebel tinnitusquestionnaire or other validated tinnitus questionnaires, audiometry,tinnitus matching, impedence, BAEP, and OAE. The improvement is anyobservable or measurable improvement. Thus, one of skill in the artrealizes that a treatment may improve the patient condition, but may notbe a complete cure of the disease.

In certain embodiments, in connection with improvement the electricalstimulation may have a “brightening” effect on the person such that theperson looks better, feels better, moves better, thinks better, andotherwise experiences an overall improvement in quality of life.

Treatment regimens may vary as well, and often depend on the health andage of the patient. Obviously, certain types of disease will requiremore aggressive treatment, while at the same time, certain patientscannot tolerate more taxing regimens. The clinician will be best suitedto make such decisions based on the known subject's history.

For purposes of this invention, beneficial or desired clinical resultsinclude, but are not limited to, alleviation of symptoms, improvement ofsymptoms, diminishment of extent of disease, stabilized (i.e., notworsening) state of disease, delay or slowing of disease progression,amelioration or palliation of the disease state, and remission (whetherpartial or total), whether objective or subjective. The improvement isany observable or measurable improvement. Thus, one of skill in the artrealizes that a treatment may improve the patient condition, but may notbe a complete cure of the disease.

VII. EXAMPLES

The following example is included to demonstrate preferred embodimentsof the invention. It should be appreciated by those of skill in the artthat the techniques disclosed in the example which follows representtechniques discovered by the inventor to function well in the practiceof the invention, and thus can be considered to constitute preferredmodes for its practice. However, those of skill in the art should, inlight of the present disclosure, appreciate that many changes can bemade in the specific embodiments which are disclosed and still obtain alike or similar result without departing from the spirit and scope ofthe invention.

Example 1 Treatment of Tinnitus

Thirteen patients with tinnitus were treated by stimulating at least oneperipheral nerve. 200 Hz, 250 microsecond pulse width pulses were usedwith amplitude dependent on an individual threshold. Of these, fournoted a decrease in tinnitus, one noted an increase and eight had noalteration in tinnitus. Tinnitus was evaluated using TMS, TENS, theGoebel tinnitus questionnaire, audiometry, tinnitus matching, impedence,BAEP, and OAE.

Example 2 Treatment of Auditory Agnosia and Tinnitus

Auditory agnosia is characterized by a relatively isolated deficit inauditory comprehension despite normal hearing. When only verbal materialis not understood, it is often called word deafness; when the deficit isin recognizing environmental sounds, it is often termed nonverbalauditory agnosia (Saygin, Dick et al. 2003).

In a patient suffering word deafness with associated complete auditoryagnosia (verbal and non-verbal) and bilateral tinnitus, TENS stimulationwas capable of attenuating the tinnitus and improving auditory agnosiaduring stimulation. In order to obtain a permanent suppression abilateral subcutaneous occipital nerve stimulation was implanted leadingto a continuous improvement of both tinnitus and auditory agnosia.

Patient History:

After a flu like syndrome a patient became comatose due to a bilateralherpes encephalitis, from which she recovered. Initially she presentedwith a complete cortical deafness, however after 3 to 4 weeks thepatient recovered partially, with almost normalized pure toneperception, but leaving her with a complete auditory agnosia andbilateral tinnitus. Language function per se is intact, with normallanguage comprehension and (motor) speech, but speech comprehension is0%. The patient can communicate via lipreading and reading. Her auditoryagnosia was complete, inclusive of a pure word deafness (=auditoryverbal agnosia). She does not recognize the sound of a barking dog, thesound of a car, she does not recognize the voice of her husband, sheonly hears sounds, perceived as a lot of chaotic noise.

Audiologic Evaluation:

Pure tone audiometry: in the right ear an average perception loss of 40dB is noted, in the left ear an average hearing loss of 50 dB

Speech audiometry: 0% for all intensities

Language analysis: normal reading, writing and language testing

Tinnitus Evaluation:

Visual Analoge Scale (intensity) rating of her tinnitus: 10/10 leftside, 5/10 right side

Tinnitus matching: polyphonic tinnitus centered around 250 dB, 40 dBabove sensorineural hearing level. Tinnitus worsens on talking, chewingand head movement (somatic tinnitus), as well as on exertion, tinnitusimproves slightly when resting. The perceived sound is described as if10 airplanes are taking off at the same time.

Tinnitus Questionnaire (Goebel and Hiller) (grade 0-4): grade 4, i.e., adecompensated severe tinnitus.

MRI Evaluation:

MRI with and without Gadolineum demonstrates thickened meninges at thetemporal lobe and contrast enhancement of the internal auditory meatus.

Functional MRI resulted in absent activation of Wernicke's area withauditory word presentation, but activation of Wernicke's area withvisual word presentation.

Treatment

The patient received transcranial magnetic stimulation at 1, 5, 10 and20 Hz. This type of stimulation did not improve the tinnitus.

Next, transcutaneous electrical nerve stimulation (TENS) was used. TENShad a beneficial effect on her tinnitus, decreasing the tinnitusintensity to 7/10 on the left side and removing the aggressivity of thesound, as well as stabilizing the tinnitus. TENS at 6 and 40 Hz, 50 μspulse width have the best effect. The patient described that thetinnitus sounds less chaotic, less fluctuating. Stress or fatiguehowever kept worsening the tinnitus, but the spontaneous variability inthe tinnitus has disappeared. After three months of TENS, the patientsfirst noticed she can recognize the sound of a car and a dog barking,but only when the TENS is on. One month later she can recognize herhusbands voice, and after one year of TENS she can recognize some words,but also only when the TENS is on.

Next, a bilateral subcutaneous occipital electrode was implanted(quatrode, ANS Medical) and connected to an internal pulse generator(Genesis, ANS Medical). This improved the tinnitus even more atstimulation settings 6 Hz, 5 μs pulse width and intensities between 2and 6 mAmp, however without auditory agnosia improvement. Stimulation at18 Hz has better effects, with even better tinnitus suppression andimmediate auditory agnosia and word deafness improvement.

Thus, electrical stimulation of the somatosensory system can be used totreat tinnitus, as well as improve auditory perception, such as auditoryagnosia and word deafness by activation of the extralemniscal auditoryconnections to the somatosensory system.

REFERENCES

All patents and publications mentioned in the specification areindicative of the levels of those skilled in the art to which theinvention pertains. All patents and publications are herein incorporatedby reference to the same extent as if each individual publication wasspecifically and individually indicated to be incorporated by reference.

-   Foxe et al., Cognitive Brain Research 10:77-83 (2000)-   Fu et al., The Journal of Neuroscience 23(20):7510-7515 (2003)-   Jones, Trends in Neuroscience, Vol. 24, No. 10:595-601 (2001)-   Moller et al., (1992), Laryngoscope. 102(10):1165-71-   Moller and Rollins, Neuroscience Letters 319:41-44 (2002)-   Moller et al., Laryngoscope 102:1165-1171 (1992)-   Mirz et al., Hearing Research 134:133-144 (1999)-   Norton, BioMedical Engineering OnLine 2:6 (2003)-   Tardif et al., Neuroscience 116:1111-1121 (2003)-   Wallhausser-Franke et al., Experimental Brain Research 153:649-654    (2003)-   Zhang et al., Experimental Brain Research 153:655-660 (2003)-   U.S. Pat. No. 5,496,369-   U.S. Pat. No. 5,697,975-   U.S. Pat. No. 5,713,847-   U.S. Pat. No. 5,735,885-   U.S. Pat. No. 5,788,656-   U.S. Pat. No. 6,210,321-   U.S. Pat. No. 6,456,886-   U.S. Pat. No. 6,656,172-   International Pub. WO 01/08617

Although the present invention and its advantages have been described indetail, it should be understood that various changes, substitutions andalterations can be made herein without departing from the invention asdefined by the appended claims. Moreover, the scope of the presentapplication is not intended to be limited to the particular embodimentsof the process, machine, manufacture, composition of matter, means,methods and steps described in the specification. As one will readilyappreciate from the disclosure, processes, machines, manufacture,compositions of matter, means, methods, or steps, presently existing orlater to be developed that perform substantially the same function orachieve substantially the same result as the corresponding embodimentsdescribed herein may be utilized. Accordingly, the appended claims areintended to include within their scope such processes, machines,manufacture, compositions of matter, means, methods, or steps.

1. A method of treating auditory dysfunction comprising the steps of:implanting at least an electrical lead within a patient such that atleast one electrode of the electrical lead is disposed adjacent to nervetissue associated with a C2 dermatome area or a C3 dermatome area;selecting a plurality of operating parameters for an electricalstimulation system that are effective for treating auditory dysfunction;programming the electrical stimulation system according to the pluralityof operating parameters; and activating the electrical stimulationsystem to deliver electrical pulses to the electrode adjacent to thenerve tissue associated with a C2 dermatome area or a C3 dermatome areathereby treating the patient's auditory dysfunction.
 2. The method ofclaim 1 wherein the nerve tissue associated with the C2 dermatome areaor C3 dermatome area comprises cranial nerves.
 3. The method of claim 1,wherein the nerve tissue associated with the C2 dermatome area or C3dermatome area comprises the occipital nerve.
 4. The method of claim 1wherein the auditory dysfunction is tinnitus, hyperacousis, phonophobia,misophonia, auditory agnosia, auditory spatial dysfunction or auditoryhallucinations.
 5. The method of claim 1 wherein the auditorydysfunction is tinnitus.
 6. The method of claim 1 wherein the auditorydysfunction is auditory agnosia.
 7. A method of treating auditorydysfunction comprising the steps of: implanting at least an electricallead within a patient such that at least one electrode of the electricallead is disposed adjacent to nerve tissue associated with a peripheralnerve selected from the group of cranial nerves consisting of olfactorynerve, optic, nerve, oculomoter nerve, trochlear nerve, trigeminalnerve, abducent nerve, facial nerve, vestibulocochlear nerve,glossopharyngeal nerve, vagal nerve, accessory nerve, hypoglossal nerve,and a combination thereof; selecting a plurality of operating parametersfor an electrical stimulation system that are effective for treatingauditory dysfunction; programming the electrical stimulation systemaccording to the plurality of operating parameters; and activating theelectrical stimulation system to deliver electrical pulses to theelectrode adjacent to the nerve tissue associated with the peripheralnerve thereby treating the patient's auditory dysfunction.
 8. The methodof claim 7 wherein the electrical stimulation delivers electrical pulseson a substantially continuous basis.
 9. The method of claim 7 whereinthe plurality of operating parameters include a pulse amplitudeparameter, a pulse width parameter, and a pulse frequency parameter. 10.The method of claim 7 wherein the pulse frequency parameter is withinthe range of about 3 to about 80 Hz.
 11. The method of claim 7 whereinthe electrical stimulation delivers electrical pulses on a temporarybasis in response to receiving an initiation signal from an externalcontrol device operated by the patient.
 12. The method of claim 7wherein the selecting comprises: temporarily delivering electricalpulses according to the plurality of operating parameters to theelectrode adjacent to the nerve tissue associated with a peripheralnerve; and monitoring the auditory dysfunction while the temporarilydelivering is performed.
 13. The method of claim 12 wherein themonitoring comprises: determining an improvement in the auditorydysfunction.
 14. The method of claim 7 wherein the auditory dysfunctionis tinnitus, hyperacousis, phonophobia, misophonia, auditory agnosia,auditory spatial dysfunction or auditory hallucinations.
 15. The methodof claim 7 wherein the lead comprises a plurality of electrodes and theplurality of operating parameters include an electrode configuration.16. The method of claim 7 further comprising adjusting stimulationparameters to optimize auditory dysfunction treatment.